read the article called the Transformation. It’s about major medical breakthroughs by: Excerpts from the article:<\/p>\n + Stein described one patient to me, a woman in her late sixties with A.M.L. She had already undergone a bone-marrow transplant, had relapsed, and then had more chemotherapy; nothing helped. To Stein\u2019s surprise, after three months on AG-221, her leukemia had gone into complete remission and her blood count had returned to normal. \u201cIt was transformative,\u201d Stein said. \u201cShe gained weight and told me that the pep in her step was back.\u201d Another patient, a sixty-year-old man with A.M.L., also had failed to benefit from several regimens of chemotherapy, and he, too, went into remission after taking AG-221. Moreover, the side effects of the medication, which is given orally, have been manageable\u2014mostly mild nausea and a loss of appetite.<\/p>\n + Advances in DNA technology and in computing led to the mapping of the healthy human genome, and of other genomes, including those of various cancers. Scientists assumed that they would soon decipher how tumors arise and find a way to stop them. In the case of some cancers, that promise has been fulfilled, but for most, especially once they have spread, it has not. In 1998, after the development of new drugs that could shut down certain cancers by choking off their blood supply\u2014an advance, known as anti-angiogenesis, that has given rise to the drug Avastin\u2014the Nobel laureate James Watson predicted that this work would \u201ccure cancer in two years.\u201d Immunotherapy has recently been shown to be highly effective against melanoma and kidney cancer, but many other cancers manage to evade this type of therapy.<\/p>\n The more scientists learn about cancer, the more diverse and vexing their opponent appears. Most cancers have several potential ways of developing. Even within a single tumor, individual cancer cells may follow separate road maps. A drug designed to target one pathway may succeed in destroying only a fraction of the tumor, leaving the rest to grow, spread, and kill. The IDH-2 mutation is just one of many enzyme mutations that are found in acute myelogenous leukemia. Recently, Timothy Ley, a researcher at Washington University, in St. Louis, and an expert on the genetics of blood cancers, published a study involving two hundred patients with A.M.L.; he found that each patient harbored a unique set of mutations. \u201cIt\u2019s complex, but I\u2019m not daunted,\u201d Ley told me. \u201cAt least now we know what we\u2019re dealing with.\u201d<\/p>\n Agios hopes that AG-221 will become a key in treating those cancers which are driven by IDH-2. In March, the company launched clinical trials of another drug, AG-120, which targets a different mutated enzyme, IDH-1. The mutation occurs in as many as ten per cent of A.M.L. patients, but it\u2019s also found in seventy per cent of patients with a type of brain tumor called a glioma and in fifty per cent of cases of cancer of the cartilage. The treatment of cancer, which traditionally adopted a destroy-the-village strategy, is becoming ever more like precision warfare. \u201cWe treat people with the specific mutation who may benefit,\u201d David Schenkein, the C.E.O. of Agios, told me. \u201cWe don\u2019t treat people who would not respond to the drug.\u201d<\/p>\n![\"NewYorkerSeptember15\"](\"https:\/\/www.technologyinvestor.com\/wp-content\/uploads\/2014\/09\/NewYorkerSeptember15.jpg\")
<\/span><\/span><\/p>\n
\n<\/span><\/span><\/p>\n![\"AGio\"](\"https:\/\/www.technologyinvestor.com\/wp-content\/uploads\/2014\/09\/AGio.jpg\")
<\/a><\/p>\n